I had surgery on my right wrist last week and it's difficult for me to type, or I would no doubt pound out another rant like the one I had about Dobermans dropping dead a few weeks ago. I can't do that today. But I still have something to say.

Here's the truth. We don't need more research about cancer. We would like cancer to be one of those things we never have to worry about, like catching a skin disease from a camel. You shouldn't need to know anything at all about cancer if you want to add a dog to your family and indeed, the average pet owner doesn't. But the breeders sure do. It "comes with the breed".

When will we declare enough already? Inbreeding is killing our beloved purebred dogs, in dozens of breed-specific ways. How can the effort to solve this problem be worse than the pain from hundreds of broken hearts? How can we profess to be "responsible" breeders yet not be horrified by the fact that we can predict the untimely deaths of the dogs we create? 

Something is very, very wrong. What we need to do is so obvious - but it won't happen.  Why? Because "breeders will never do it".

Dogs chose to join us tens of thousands of years ago in a most remarkable partnership. Dogs truly are God's gift to mankind. If not for them, the trajectory of civilization would be very different. And what would we be without dogs as our best friends? What would your life be like without dogs?

I'm really, really sad. And really, really mad. Everyone offers condolences. "They're never with us long enough", and "I feel your pain", and "Remember the wonderful memories". And I too, am so, so sorry. But damn it, THIS IS NOT OKAY.

Only the breeders can fix this. Enough already. Get it done.
​

The internet is a wonderful thing. Everything known in the universe can be researched from a laptop computer. However, anybody with a laptop can post whatever they want and call it "information". For some stuff, it really does matter if it's wrong.

Here's this post about hip dysplasia, by Dr Jeannie, Animal Naturopath, part of which I have posted below. 

4) "Hip dysplasia is not a congenital defect; it is not present at birth. Multiple studies have demonstrated that all normal puppies are born with “perfect” hips; that is, they are “normal” for a newborn, with no signs of dysplasia. The structures of the hip joint are cartilage at birth and only become bone as the puppy grows. If a puppy is going to develop hip dysplasia, the process begins shortly after birth."

This statement is TRUE. In fact, it is copied - word for word, cut-and-paste - from my blog post on the topic, without citation or quotes to indicate that it is copied.

(pla·gia·rism - noun
synonyms:copying, infringement of copyright, piracy, theft, stealing; "wrongful appropriation" and "stealing and publication" of another author's "language, thoughts, ideas, or expressions" and the representation of them as one's own original work.)

Statement #4 is TRUE, but plagiarized from me. Yes, Dr Jeannie, plagiarist.

5) "Exercise is good and bad!  Exercise strengthens the muscles of the legs and pelvis, and this will increase the stability of the hip joint. But not all exercise is created equal.Puppies raised on slippery surfaces or with access to stairs when they are less than 3 months old have a higher risk of hip dysplasia,while those who are allowed off-lead exercise on soft, uneven ground (such as in a large yard or  park) have a lower risk (Krontveit et al 2012). Dogs born in the summer have a lower risk of hip dysplasia, presumably because they have more opportunity for exercise outdoors (Ktontveit et al 2012) in the sunshine, fresh air and on dirt! On the other hand, dogs from 12-24 months old that regularly chase a ball or stick thrown by the owner have been found to have a higher risk of developing dysplastic hips (Sallander et al 2006).
The most critical period for proper growth and development of the hip in dogs is from birth to 8 weeks old, so the type of exercise the puppies are exposed to is most important during this time."

Oh my. ​All of this, of course is true, because it's an even bigger chunk of MY text, copied wholesale and without attribution, by Dr Jeannie for you to ponder. (Note that she even copied the sources I included in my post!).

6) This one is my favorite. First, read what I wrote.

"Nutrition is important
While puppies are growing rapidly, it is critically important to get their nutrition right.

Growing puppies need to eat enough to support growth but they should not be fat, because any extra weight can increase the risk of developing hip dysplasia (Hedhammar et al 1975, Kasstrom 1975). An additional problem is that puppies getting too much food could also consume too much of specific nutrients. Puppies provided a quality commercial puppy food that is fed in the proper amount will have a nutritionally balanced diet and should not receive any supplements. Dietary supplements, especially of calcium, are not only unnecessary but could cause serious problems. There is no evidence that supplemental protein or vitamins will reduce the risk of hip dysplasia (Kealy et al 1991, Nap et al 1991, Richardson & Zentek 1998)."

Now, read what Dr Jeannie wrote:

"Nutrition is Important
While puppies are growing rapidly, it is critically important to get their nutrition correct. What better nutrition can there be then what is found in a species specific diet – Dogs being carnivores, will thrive on a raw meat, bone and organ diet.
Some little known facts for you to think about:
by Dr. Tom Hungerford.
By 1965, a mere 30 years later… Hip Dysplasia was identified in 55 breeds world-wide. And the skeletal problems didn’t stop there.
Think about this, how do you think it is that CHD (Canine hip Dysplasia) and later more structural issues could suddenly appear in just 30 years and spread rapidly through all breeds?
Did Hip and Elbow Dysplasia exist before 1935? If so, was it common?
If it were not in existence, where did it come from, what happened?
What does all of this mean if we are assuming that these diseases are inherited and can therefore be eliminated by genetic means? We’ve been trying to breed this out for 50 years and have not yet been really successful!
So if CHD truly is genetic in nature, then the genes which cause it, have had to have always been present in the dog population but were only “switched on” somehow in 30 short years. What happened after the 1930’s?
Commercial Dog food emerged!
Up until the early 1940’s, people fed their pets on food scraps and raw meaty bones.Since the early 40’s, disease in our pets has shifted drastically! The widespread, across the board switch to processed commercial foods has resulted in a catastrophic increase in not only skeletal diseases but liver disease, pancreatic disease and cancer!"

At last, we see now why Dr Jeannie, plagiarist, thinks hip dysplasia can't be genetic- or if it is, those genes have been "turned on" by "processed commercial dog food". It's because "dogs being carnivores", they should be on a raw diet. 

Yes, nutrition is important. But nothing else in Dr Jeannie, plagiarist's statement is supported by even the tiniest shred of documented fact. Dogs and wolves are the same species, but their nutritional needs are very different. In fact, the digestive enzymes of dogs reflect their adaptation during domestication to a diet that is omnivorous and higher in starch, and very different than that of wolves. No, the "ideal" diet for a dog is not raw, meaty bones, and their digestive enzymes are the proof. You don't have to take my word for it; you can download the most recent paper, published just last month, below. The notion that dogs and wolves should have the same diet is soundly refuted by science, and those that continue to claim this are purporting belief, not fact. Beliefs are what fairy tales are made of.

Oddly, Dr Jeannie does not provide a citation or source for her "information" apparently attributed to Dr Hungerford. However, a quick search on the internet turns up references to him dating in the 1930's, long before we knew much about either hip dysplasia or physiological adaptations of domesticated dogs to diet. This seemed odd to me, given the reference in the post to 1965.

But mystery solved. This is a bit of confusion caused by yet another of (plagiarist) Dr Jeannie's sloppy cut-and-paste jobs, this time from the Endless Mtn Labrador website, which I post here for your comparison:

"Hip Dysplasia was the first juvenile Bone Disease recognized in dogs, in 1935 by Dr. Tom Hungerford. By 1965, a mere 30 years later…
Hip Dysplasia was identified in 55 breeds world-wide. And the skeletal problems didn’t stop there. Other problems emerged with the shoulders, elbows, hock, and stifle.
So here’s some questions no one is asking:
-How is it that HD (Hip Dysplasia) and later structural issues could suddenly appear and spread rapidly through all breeds?
-Did Hip and Elbow Dysplasia exist before 1935? If so, was it common?
-If they were not in existence, where did they come from?
-Why can’t we eliminate these problems despite mass radiology and mass culling?
-What does all of this mean if we are assuming that these diseases are inherited and can therefore be eliminated by genetic means? We’ve been trying to breed this out for 50 years and have not been successful! (except for various reputable kennels who have decades of genetic clearances!)
So if HD and ED are genetic in nature, it must be that the genes which cause them have always been present in the dog population. So what OTHER factors are causing these skeletal diseases?? What happened after the 1930’s?
Commercial Dog food emerged!"

​Oops. You can see now that poor Dr Hungerford didn't say any of those things that appear to be attributed to him in plagiaristDr Jennie's post. And Dr Jeannie didn't say any of the things that should in fact have been attributed to the Endless Mtn Labrador website - and since nobody but me is providing attributions of any sort, who knows  where any of this stuff actually came from. 

To cap it all off, plagiarist Dr Jeannie's website contains a long page of disclaimers and this truly remarkable statement:

"Articles written by Dr. Jeannie (Jeanette) Thomason may NOT be reprinted without express written permission and then printed in their entirety only and with following attribution box intact and hyperlinked: Dr. Jeannie Thomason is a certified animal naturopath and a proficient blogger and writer on natural pet health. She worked in traditional veterinary medicine for many years and continues to do extensive research into natural health care for dogs, cats and parrots..All rights reserved. No part of this article may be reproduced in any form without the written consent of the Author. This article is for educational purposes only. The decision to use, or not to use, any information is the sole responsibility of the reader."

Dr Jeannie, not only have you have most definitely violated my copyright, but you managed to even plagiarize badly. ("proficient" blogger???)  You can remove your embarassing post from your "Whole Dog Website", but I have reproduced enough of it here that anybody who wishes will be able to evaluate the "quality" of your work. Or, for those that want the complete experience, here's a pdf.

PS I am unable to find any accredited institution that offers a "doctorate" in "veterinary naturopathy", as Dr Jeannie (Thomason) claims to have, and she (oddly) does not divulge where she got this degree. It is not a recognized veterinary specialty.

Genetic drift results in the loss of genetic diversity and an increase in inbreeding over time, and the rates of both of these processes depends on population size:

Rate (inbreeding or genetic drift) = 1/2Ne

where Ne is "effective population size", which we will define shortly.

As an example, if we have a population of 10 breeding animals, the rate of inbreeding will be 1/(2 x 10) = 1/20 = 0.05. As a percentage, that would be a 5% increase in homozygosity per generation, which is very high. What if the population size is 100? The rate of inbreeding would be 1/(2 x 100) = 0.005, or 0.5% increase in homozygosity per generation. For genetic diversity, the calculations are the same, and the value is the amount of genetic diversity (as a fraction or a percentage) lost per generation.

So, the rates of inbreeding and of genetic drift per generation will increase as Ne gets smaller.

EFFECTIVE POPULATION SIZE
If you are managing groups of animals, you might want to understand how the size of a particular population will affect genetics. The easiest way to do this is to pretend you have an "ideal" population that meets certain criteria:

a) The number of males and females is equal and all can reproduce;

b) All animals are equally likely to produce offspring, and the number each produces varies no more than expected by chance;

c) Mating is random (remember Hardy-Weinberg?);

d) The number of breeding animals is the same from one generation to the next (i.e., the population size is constant) and there is no immigration, emigration, mutation, or selection.

For this ideal population, we can determine something called "effective population size", Ne.

In an "ideal" population (one that meets the criteria listed above), the census population size and the effective population size are equal. But most real populations violate at least some of the criteria for an ideal population (e.g., sex ratios are not equal, breeding is not random, etc), and for them the effective population size is less than the census size.

If real populations are rarely ideal, what's the point of having something called effective population size? The genetics of ideal populations are predictable. If we could describe our herd with a census size of 10,000 antelope in terms of effective population size, we could make predictions about how it would behave genetically. How can we get from census size, Nc, to Ne?

There are several ways to estimate Ne for a population, depending upon the data available and the type of estimation you're trying to make.

First, let's produce a formal definition of Ne:

Effective population size is the size of an "ideal" population of animals that would have the same rate of inbreeding or decrease in genetic diversity due to genetic drift as the real population of interest.

Effect of sex ratio on Ne
There are several different ways to compute Ne. We will look only at one here that is easy for breeders to use.
One of the things that can influence the effective population size is the sex ratio of the breeding animals.

We can estimate Ne using information from a population census or pedigree database about the numbers of males (Nm) and females (Nf) that produce offspring in a generation.

Ne = 4 x (Nm x Nf) / (Nm + Nf)

The denominator (bottom) of this equation is the number of males plus the number of females (Nm + Nf), which is simply the total number of breeding animals. The numerator (top) of the equation is four times the product of Nm and Nf (4 x (Nm x Nf)).

A simple example
Let's say we have a population of 10 animals, 5 males and 5 females. The effective population size Ne would be

Ne = 4 x (5 x 5) / (5 + 5)

Ne = 4 x 25/10 = 10

See that? When we had equal numbers of males and females, Ne is the same as the census size. Try working a few of these with other population sizes, but always with equal numbers of males and females.

As you know, the number of breeding males and females in purebred dog populations are rarely equal, with the number of females usually being greater because males can sire multiple litters. What happens to the effective population size when the sex ratio of breeding animals is not equal?

An extreme example
Let's just cut to the chase and create a crazy population of animals, with 1000 females and just 1 male. For this, the math will be:

Ne = 4 x (1000 x 1) / (1000 + 1) = 4 x 1000/1001 = 3.996, or approximately = 4.

Wow. We have 1,001 animals, but the effective population size is FOUR.

We had a herd of 1,000 animals, and because we used only one male for breeding, our population is going to behave genetically AS IF it is a population of only 4 animals, two males and two females.

What if there are 1,000 males and only one female? Apart from the awkward logistics, the result in terms of genetics will be the same. The Ne will again be approximately 4.

As you can see, an imbalance in the number of breeding males and females will affect the estimate of Ne. How big this effect is will depend on the size of the population and the sex ratio.
​
Let's look at this graph, which is for a population with a total of 1,000 animals. The number of females (Nf) is on the x-axis, and the number of males is not displayed but inferred by subtraction (Nm = 1000 - Nf). When the number of males and females is equal (i.e., Nf = Nm = 500), the effective population size (Ne) equals 1,000; i.e., Ne is the same as the census population size.

​When the number of females (Nf) is 800 (so the number of males (Nm) is 200 by difference), the resulting effective population size from the graph is about 650. If the number of breeding males is reduced to 100, Nf will be 900 and Ne will be about 350. The curve is symmetrical; you can run similar examples with small Nf and large Nm, and the resulting Ne will be the same.

What you can see here is that when the sex ratio of breeding animals is not 1:1, the Ne is reduced, meaning that rates of inbreeding and genetic drift will be similar to the ones you would expect to see in a population of smaller size. Furthermore, the more extreme the ratio, the greater the effect on the genetics of the population.

I'm sure you can see the problem here. Inbreeding and loss of genetic diversity result in an increase in inbreeding depression and the expression of recessive mutations. Litter sizes get smaller, puppy mortality goes up, lifespan is shortened, and unhealthy animals are removed from the breeding stock. Reducing the number of breeding animals will cause the rates of inbreeding and genetic drift to increase, which will increase inbreeding depression and the expression of genetic diseases, which will reduce the number of breeding animals...and you can see where this is going. This phenomenon is called the "extinction vortex".

You can also see how allowing only a few of the males to breed (or a popular sire) will affect the gene pool. While breeders think they are improving genetic health by using only the very best dogs for studs, the result is that inbreeding and loss of genetic diversity will both increase, and you will end up in the extinction vortex.

There are consequences here for spay/neuter policies and breeding contracts. Removal of animals from the breeding population makes it more difficult for breeders to manage the rate of inbreeding, and higher levels of genetic drift cause genetic instability, with larger fluctuations in allele frequencies and greater risk of extinction.
​
This raises an important consideration when using information from DNA trait and mutation tests and genotyping (e.g., MyDogDNA, UC Davis diversity test) to make breeding decisions. Breeders are able to improve breeding decisions through careful mate selection using DNA information, but if the sex ratio of breeding animals is strongly unbalanced or the size of the breeding population is too small, inbreeding and loss of genetic diversity will be working in the opposite direction, compromising the health of the gene pool. Genotyping can help improve the quality of the next litter, but reducing the incidence of genetic disorders in a breed will require appropriate genetic management of the entire population using breeding strategies that will limit the rate of inbreeding and loss of genetic diversity. In fact, if breeders are not keeping an eye on the larger picture, these tests might cause breeders to be even more selective in their breeding choices, with deleterious long term consequnces. In fact, this is what happened when genomic testing was first introduced to livestock breeding. Selecting only the best animals for breeding based on DNA increased the rate of inbreeding and loss of genetic diversity, producing short term gain but damaging the gene pool. There is no silver bullet that will cure all problems. Breed-level genetic management is essential to maintain the health of the gene pool over the long term.

Breeders should know the effective population size of their breed, and they should understand the things they can do to increase it. Larger Ne will improve genetic stability and the health of the gene pool; smaller Ne will result in unpredictable variation in allele frequencies, loss or fixation of some alleles, and an increase the risk of extinction. You can see how I was able to use information from the UK Kennel Club stud books to estimate effective population sizes of dog breeds in the UK and particularly of terriers, and from this produce lists of breeds at risk of extinction.

Although Ne is not especially hard to compute with the formula that was used here, there is an online calculator that will allow you to experiment with sex ratio and population size: Effective Population Size Calculator.

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By Carol Beuchat PhD

There is a most unusual cancer that occurs only in dogs. Not only is it contagious, it is also the oldest cancer in the world.

By oldest, I don't mean we've known about it the longest. When a dog has this form of cancer, the tumor cells themselves are 11,000 years old!

The cancer is canine transmissible venereal tumor (CTVT), and it was first described by a Russian veterinarian named Mstislav Novinski in the 1870s. It is called a transmissible cancer because it is contagious, having the unusual ability to be spread from dog to dog when cancer cells are transferred during mating or other contact. The original cancerous cells occurred in a single dog about 11,000 years ago and, instead of dying when the dog died, the cancer spread from dog to dog contagiously. It is now can be found in dog populations around the world.

Strakova A, MN Leathlobhair, G-D Wang, and many others. 2016. Mitochondrial genetic diversity, selection and recombination in a canine transmissible cancer. eLife 2016;5:e14552.DOI: http://dx.doi.org/10.7554/eLife.14552

You can learn more Really Cool Stuff about dogs in ICBs new course!

The Biology of Dogs

Online course starts 15 August 2016!

Join us!

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​